This project is concerned with the epidemiological aspects of S. mutans transmission within families. Previous investigators studying both animal models and human volunteers have suggested mothers to be major source of S. mutans to their infants. Evidence comes from observed similarities among strains of S. mutans as determined by serotyping, biotyping and bacteriocin profiles. Unfortunately, these methods have major limitations. In this project we are using plasmid DNA as a stable epidemiological marker for ascertaining homology of strains of S. mutans among mothers and other family members, and between mothers and their children. In addition, we are also developing more sensitive bacteriocin typing methods to use along with plasmid profile to examine homology of strains within family units. We are currently exploring cell protein and chromosomal DNA profile methods for ascertaining homology in strains not having plasmid DNA. To date, we have examined strains of S. mutans from approximately 300 select mother-child pairs and in depth family profiles on 10 of these pairs in which one member was positive for plasmid DNA. The significance of this study comes from the prospect of being able to identify the source of S. mutans acquired by an infant and then devise ways of interfering with transmission, hence preventing dental caries. Also, this study allows us to explore the genetic aspects of S. mutans to determine possible virulence factors associated with plasmid DNA.